Sr62 Wheat tandem kinase-NLR
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB74232 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR12796602_1.fastq.gz | Fastqsanger.gz | |||
| ERR12796602_2.fastq.gz | Fastqsanger.gz | |||
| ERR12799903_1.fastq.gz | Fastqsanger.gz | |||
| ERR12799903_2.fastq.gz | Fastqsanger.gz |
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Project description:Plants growing in soil are challenged by multiple biotic (e.g. pathogens) and abiotic (e.g. heavy metals) stressors. Stress resistance is a key determinant for plants to thrive in the environment. Resistance to pathogens requires innate immunity 1, whereas tolerance to metal ions is accomplished by mechanisms such as complexation and compartmentation2,3. Some transition metals can enhance plant’s defense against pathogens4,5, but the mechanism remains unclear. Here, we show that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors antagonistically control transition metal-triggered immunity. One NLR, STM2 directly perceives transition metal ions, such as Cd2+, Cu2+ and Zn2+, as a ligand to activate its NAD+ hydrolytic activity and immune responses, triggering enhanced resistance to the soil-borne bacterial wilt pathogen Ralstonia solanacearum. The other NLR, STM1 suppresses STM2 to protect plants from transition metal-triggered immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between resistance to pathogens and tolerance to transition metals that are pervasive in soil.
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Project description:Plants growing in soil are challenged by multiple biotic (e.g. pathogens) and abiotic (e.g. heavy metals) stressors. Stress resistance is a key determinant for plants to thrive in the environment. Resistance to pathogens requires innate immunity , whereas tolerance to metal ions is accomplished by mechanisms such as complexation and compartmentation. Some transition metals can enhance plant’s defense against pathogens4,5, but the mechanism remains unclear. Here, we show that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors antagonistically control transition metal-triggered immunity. One NLR, STM2 directly perceives transition metal ions, such as Cd2+, Cu2+ and Zn2+, as a ligand to activate its NAD+ hydrolytic activity and immune responses, triggering enhanced resistance to the soil-borne bacterial wilt pathogen Ralstonia solanacearum. The other NLR, STM1 suppresses STM2 to protect plants from transition metal-triggered immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between resistance to pathogens and tolerance to transition metals that are pervasive in soil.
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Project description:Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. During plant development and especially during aging, fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Although individual mutations in NLRs, PRRs or other immune-related components that interact with catalytically inactive AtMC1 do not rescue the autoimmune phenotype, overexpression of SNIPER1, a master regulator of NLR homeostasis, fully attenuates the phenotype, inferring that a broad defect in NLR turnover may underlie the severe autoimmunity observed. As opposed to Wt AtMC1 which exhibits a nucleocytoplasmic localization, catalytically inactive AtMC1 localizes to puncta structures that are degraded through autophagy. We infer that the phenotypes observed in plants overexpressing catalytically inactive AtMC1 may represent an additive phenotype to the relatively milder autoimmunity observed in atmc1 mutants. Altogether and considering previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels as plants approach adulthood, thus preventing autoimmunity.
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Project description:Characterization of NWD1; a novel NLR-related protein and further correlate it as a putative Prostate Cancer marker. NLRs (NACHT and Leucine Rich Repeat domain containing proteins) constitute a major subfamily of innate immunity proteins mostly acting as cytosolic pattern recognition receptors (PRRs), involved in the detection of cytoplasmic pathogen-associated molecular patterns (PAMPs) and endogenous danger signals. The recognition of the signals initiates a variety of host defense pathways through the activation of NF-kappaB, stress kinases, interferon response factors (IRFs) and/or inflammatory caspases. Despite the importance in host immune response, deregulation on NLR activities has been described in a variety of maladies, including chronic inflammation and cancer predisposition. For instance, NOD1 was one of the first NLR members shown to possibly play a role in tumorigenesis, since NOD1 stimulation induces apoptosis in MCF-7 breast carcinoma cells, and NOD1-/- MCF-7 cells generate larger tumors after injection in SCID mice. Mice deficient in NLR member NLRP3, and/or its interacting partners ASC or caspase-1, are also shown to be more susceptible to colitis-associated cancer (CAC). Polymorphisms along NLR genes NOD1 and NOD2 have also been correlated with altered cancer risk. NOD1 SNPs have been associated with gastric cancer, lymphoma, ovarian, prostate, and lung cancer due to the recognition of H. pylori (etiologic agent in gastric cancer and MALT lymphoma), C. trachomatis (putative etiologic agent in ovarian cancer), P. acnes (possible causative agent in PCa) and C. pneumonia (plausible etiological agent in lung cancer) as NOD1 ligands. Particularly, NOD1 and NOD2 have been shown to be fully operative in prostate epithelial cells and, in cooperation with TLRs, may elicit immune response during PCa progression. To access a tissue-specific gene expression profile for NWD1, quantitative PCR analysis was performed using a normalized cDNA panel derived from 48 human tissues (TissueScan Tissue qPCR Array, Origene). Two apparently independent expression patterns were detected, respectively related to neurological related organs (brain, pituitary and retina) and male reproductive system (prostate, epididymis and testis), where the highest mRNA levels was observed in prostate tissue. Results were confirmed using a second set of NWD1-specific qPCR primers (data not shown). Moreover, a similar expression pattern was virtually observed using the SAGE database from the Cancer Genome Anatomy Project (CGAP) of the National Cancer Institute (not shown). Comparative gene expression microarray data was analyzed systematically by Ingenuity Pathway Analysis (IPA) to set up potential networks based on NWD1 regulated genes. The eventual participation of NWD1 in signaling transduction pathways was further examined by microarray analysis (Human WG-6v3 Expression BeadChip, Illumina) comparing the expression profile of PPC-1 cells lacking NWD1 expression (sh184 & sh3922) versus control cells (shGFP). According to the differential expression profile that was generated and analyzed by the Ingenuity PathwaysTM software (IPA version 7.1, Ingenuity Systems), NWD1 is presumably associated with biological networks related, for instance, to tissue morphology, organogenesis, cancer and neurological diseases .
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Project description:Characterization of NWD1; a novel NLR-related protein and further correlate it as a putative Prostate Cancer marker. NLRs (NACHT and Leucine Rich Repeat domain containing proteins) constitute a major subfamily of innate immunity proteins mostly acting as cytosolic pattern recognition receptors (PRRs), involved in the detection of cytoplasmic pathogen-associated molecular patterns (PAMPs) and endogenous danger signals. The recognition of the signals initiates a variety of host defense pathways through the activation of NF-kappaB, stress kinases, interferon response factors (IRFs) and/or inflammatory caspases. Despite the importance in host immune response, deregulation on NLR activities has been described in a variety of maladies, including chronic inflammation and cancer predisposition. For instance, NOD1 was one of the first NLR members shown to possibly play a role in tumorigenesis, since NOD1 stimulation induces apoptosis in MCF-7 breast carcinoma cells, and NOD1-/- MCF-7 cells generate larger tumors after injection in SCID mice. Mice deficient in NLR member NLRP3, and/or its interacting partners ASC or caspase-1, are also shown to be more susceptible to colitis-associated cancer (CAC). Polymorphisms along NLR genes NOD1 and NOD2 have also been correlated with altered cancer risk. NOD1 SNPs have been associated with gastric cancer, lymphoma, ovarian, prostate, and lung cancer due to the recognition of H. pylori (etiologic agent in gastric cancer and MALT lymphoma), C. trachomatis (putative etiologic agent in ovarian cancer), P. acnes (possible causative agent in PCa) and C. pneumonia (plausible etiological agent in lung cancer) as NOD1 ligands. Particularly, NOD1 and NOD2 have been shown to be fully operative in prostate epithelial cells and, in cooperation with TLRs, may elicit immune response during PCa progression.
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